Effect of anemia on oxygen transport in hemorrhagic shock

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Abstract
Effect of anemia on tolerance of hemorrhagic shock in rats was studied to examine opposing effects of altered O2 capacity and viscosity of O2 delivery at reduced blood flow. Hematocrit [Hct] was 1st reduced by exchange transfusion. Hypotension (BP [blood pressure] = 30 torr) was induced and maintained at this level by controlled hemorrhage; it was terminated when reinfusion of shed blood became necessary to sustain this blood pressure. The period of compensation (time at 30 torr until reinfusion) in control rats (Hct = 42.5 .+-. 2.7%) was 59 .+-. 23 min; in anemic rats (Hct = 23.3 .+-. 2.2%) it was 53 .+-. 15 min (SD, P = 0.086). Bleeding rate during shock, mortality, .ovrhdot.VO2 [O2 consumption], acid-base balance, and mortality were not influenced by anemia, except for slightly higher lactate in late shock in anemia. The lack of influence of anemia (cf. other perturbations of O2 transport) was apparently due to a 59-88% increase in cardiac output during shock in anemia, which maintained .ovrhdot.VO2.